The incubation of Streptococcus gordonii DL1 with polymorphonuclear leukocytes (PMNs) resulted in the stimulation of the production of superoxide anions, the release of the contents of PMN primary granules and the ingestion of the bacteria. These responses were inhibited by pronase treatment of the bacteria, sialidase treatment of PMNs or inclusion of N- acetylneuraminlactose in the incubation mixtures. Thus, the interaction of a sialic acid reactive bacterial lectin with PMN glycoconjugate receptors was implicated. In contrast to previously described interactions of bacterial lectins with phagocytic cells, S. gordonii DL1 was not killed. These microorganisms were not inherently resistant to the bactericidal activity of PMNs since streptococci preincubated with antibody prior to the addition of PMNs were destroyed, an effect that was significantly enhanced by the addition of complement. A strain lacking the sialic acid reactive lectin, S. gordonii M5, failed to activate PMNs. Six additional strains of S. gordonii that possessed sialic acid reactive lectins all stimulated the release of superoxide anions. Of these, two were resistant to the bactericidal effects of PMNs. However, the viability of two strains was reduced 80-90% following incubation with PMNs and approximately 40% lectin dependent killing by PMNs was achieved with the other two strains. Since oral viridans streptococci are etiological agents of bacterial endocarditis, studies have been initiated to determine if these lectin mediated interactions of streptococci with PMNs may influence the induction of this disease process. A rat model of endocarditis has been established in which the aortic valve is damaged by insertion of a catheter. Those strains that were killed by PMNs failed to initiate the disease but, of major interest, those that evaded PMN intracellular killing induced endocarditis. In the latter case the lectin-mediated ingestion of the bacteria may actually prevent clearance of the microorganisms thereby favoring colonization of cardiac valves. Thus, the resistance to PMN dependent bactericidal activity appears to be an important determinant of virulence.